Hypocalcemia in the intensive care unit manifests primarily through neuromuscular excitation—including seizures, paresthesias, and tetany—and cardiovascular instability, such as refractory hypotension and QT prolongation. Total serum calcium serves only as a crude screening tool, as ionized calcium provides the only physiologically relevant measurement. Clinicians must account for potential artifacts, such as false-low readings following gadolinium-enhanced MRI scans. While severe, symptomatic cases require intravenous repletion, aggressive correction of mild, asymptomatic hypocalcemia remains unsupported by evidence and may be counterproductive. Management should prioritize identifying underlying drivers like hypomagnesemia, massive transfusion-related citrate toxicity, or severe inflammation. Ultimately, clinical focus should remain on patient symptoms rather than chasing arbitrary laboratory thresholds, as mild hypocalcemia is frequently an epiphenomenon of critical illness rather than a primary driver of morbidity.
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